biostudies-literatureGarcia-Lopez MAMinisterio de Ciencia e Innovación (MCIN)Fundación BBVAComunidad de MadridMinisterio de Ciencia e InnovaciónFundación BBVA (FBBVA)Comunidad de Madrid (Community of Madrid)e2300096121https://www.ebi.ac.uk/biostudies/studies/S-EPMC10801893biostudies-literatureUnknown121(3)The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue (AT), the main fat storage organ with endocrine capacity, plays fundamental roles in systemic metabolism and obesity-related diseases. Dysfunctional AT can induce excess or reduced body fat (lipodystrophy). <i>Dido1</i> is a marker gene for stemness; gene-targeting experiments compromised several functions ranging from cell division to embryonic stem cell differentiation, both in vivo and in vitro. We report that mutant mice lacking the DIDO N terminus show a lean phenotype. This consists of reduced AT and hypolipidemia, even when mice are fProceedings of the National Academy of Sciences of the United States of AmericaDIDO is necessary for the adipogenesis that promotes diet-induced obesity.PMC10801893S2017/BMD-3804PID2022-142616OB-100&quot;The role of Dido...&quot;PID2019-110574RB-100"The role of Dido..."Sabio GFischer TMora ASanchez de Diego ATalavera Gutierrez AGarcia-Lopez MAMedina-Gomez GPons TMartinez-A CCorrales Pvan Wely KHMfalseDIDO is necessary for the adipogenesis that promotes diet-induced obesity.The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue (AT), the main fat storage organ with endocrine capacity, plays fundamental roles in systemic metabolism and obesity-related diseases. Dysfunctional AT can induce excess or reduced body fat (lipodystrophy). <i>Dido1</i> is a marker gene for stemness; gene-targeting experiments compromised several functions ranging from cell division to embryonic stem cell differentiation, both in vivo and in vitro. We report that mutant mice lacking the DIDO N terminus show a lean phenotype. This consists of reduced AT and hypolipidemia, even when mice are f2024-01-01T00:00:00Z2024 Jan2026-07-15T05:14:47.169Z2025-04-04T11:24:42.732ZS-EPMC108018933819445710.1073/pnas.2300096121